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Lectures of 'From Perception to Consciousness', part one. €7,39   In winkelwagen

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Lectures of 'From Perception to Consciousness', part one.

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These are notes of all the lectures of the first part of From Perception to Consciousness. Please note that this should be used as a study tool! Don't rely solely on these notes, and do some studying yourself.

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  • 19 februari 2021
  • 59
  • 2020/2021
  • College aantekeningen
  • Victor lamme
  • Alle colleges
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psychmeisje
B&C: from perception to consciousness


Lecture one: The Retina
Lecture two: The Visual Cortex pt. 1
Lecture three: The Visual Cortex pt. 2
Lecture four: The Visual Cortex pt. 3
Lecture five: Perceptual Organization
Lecture six: Are Faces Special?
Lecture seven: Object Recognition
Lecture eight: Action
Lecture nine: Q&A and Trial Exam Questions

,Lecture one: The Retina
Monday the 1st of February, 13.00 – 15.00, Victor Lamme


The retina

The retina is an apparatus that looks a bit like a camera. Something from the outside is
projected via the lens, on the back of the eye, where the retina is. In the retina, the
image is sampled by the rods and cones.


The retina1
The retina contains the neuro-component of the eye. The cellular layers of the retina
contain cells that detect and respond to light, and they are called photoreceptors. There are
two types:
 Rods. They allow us to see in dim light, but don’t allow for perception or color.
 Cones. They allow us to perceive color under normal lighting conditions.

Throughout most of the retina, rods outnumber cones. However, in one area, the fovea,
there are no rods and many cones. The fovea represents the area of our retina that provides
our sharpest vision, and this is at the center of our gaze.

The signal of light is transmitted to bipolar cells, which connect the photoreceptors to
ganglion cells. This leaves the eye in a large cluster: the optic disc. The optic disc doesn’t
contain photoreceptors, and cannot process visual information, creating the blind spot. We
normally don’t notice our blind spot, because our brains fill in the gap.

After leaving the retina, the ganglion cell fibers are called the optic nerve. The optic nerve
carries visual information to the brain to be processed. Two other kinds of cells:
 Horizontal cells: receive input from multiple photoreceptor cells.
 Amacrine cells: receive signals from bipolar cells.




The retina processes the rod and cone signals via bipolar cells to ganglion cells. The
ganglion cells pass the preprocessed signals to the brain. The retina can be seen as a
piece of brain, outside of the brain. It is a piece of neural tissue that is preprocessing the
image from the rods and cones. It does this with a small network of bipolar cells,
ganglion cells, horizontal cells and amacrine cells. This network, in combination,
processes the images, and sends it to the optic nerve and then to the brain.


Rods and cones

Rods and cones are sensitive to different wave lengths. There are three types of cones:
 Short-wavelength cones: respond best to blue. This is 419 nm.
 Medium-wavelength cones: respond best to green. This is 531 nm.
 Long-wavelength cones: respond best to red or yellow. This is 559 nm.

Rods are sensitive to an intermediate wavelength, of 496 nm, which is in the green-ish
part of the spectrum. These rods and cones transform the light into a neural signal. They
use a protein for this: called rhodopsin in rods, and photopsin in cones. If this protein is
activated by light, it activates a bunch of other proteins, and then you get a signal

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,cascade, which leads to the closing of a sodium channel. The membrane then
hyperpolarizes, which leads to a neural signal that is sent to the bipolar cells, and then
to ganglion cells.

Different rhodopsins/photopsins are sensitive to different wavelengths. There are many
varieties in the animal kingdom. Humans have four different kinds (three for cones, one
for rods), while other animals have three or five. This means that colors that we see as
the same color, are different colors for some animals.


Retinal color blindness

This exist when there is an absence of a particular
cone type. This is studied with ishihara plates. People
with normal color vision can see an 8, but when you
have retinal color blindness, you see a 3. Color
blindness is not uncommon among humans. 8% of
Caucasian males, 5% of Asian males, and 3% of
African males are colorblind. The probability in
females is ten times less.



The fovea

The cones are primarily present in the central part of the retina: the fovea. The fovea is
tightly packed with cones, there are no rods there. This is the place where you have
sharp, color vision. The rods are mostly present in the para-fovea (or the periphery of
your vision).

The fovea is a cup-shaped thing, with the highest density of photoreceptors, mainly
cones. The fundus is the back of your eye, and you can not only the fovea, but also a lot
of blood vessels. Your retina is covered with blood vessels, but you don’t see those,
mostly because of the fact that your eyes adapt to them. There are also particles
(“bugs”) in your peripheral vision, which are proteins or small blood leaks that float in
your vitreous body: the mass of substance that is filling the rest of the eye. This is an
obstacle for light going to the photoreceptors. You can see the veins in your eyes if you
close your eyes, and hold a light source to the side of your eye. Then wiggle the light up
and down.

Macular degeneration
There are some diseases which affect the fovea. Examples are Dry Macular Degeneration
and Wet Macular Degeneration. There is protein, or other deposits, occurring in the
retina, and this shreds the cells apart. This disease comes with old age, and smoking and
diet influence it. The macula (≈ fovea) is affected, and you get problems with central,
foveal, vision. You may get distortion or even a hole in the center of your vision. There
are some treatments, but it is difficult to control.


Pigment epithelium

So, light has to pass through blood vessels, to go to the retina. But it also has to pass
the retinal network itself, to reach the photoreceptors. The receptors are in the back of
the eye, but the ganglion cells, bipolar cells, horizontal cells and amacrine cells are in
front of that. The light has to pass through the network to reach the photoreceptors. The
reason for this difficulty is that in the back, there is a layer called the (retinal) pigment
epithelium (RPE). It is full of granules with pigment, and they absorb the light. If you

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, would not have that, and light would just hit the photoreceptors, the light would be
reflected and scattered back. Anything in the world reflects light. Then, the signal would
just scatter and activate other photoreceptors all over the place. The RPE prevents this,
so that the light is only activating a particular photoreceptor. This means that you can
have really sharp vision. That is also why these photoreceptors are sitting in the back,
embedded in the RPE. RPE also provides nutrients for photoreceptors, which consume
quite a lot of energy.

There are animals who don’t have this, but who have a layer that reflects the light. Cats,
for example, have pigment epithelium that is light reflective instead of absorbent. Cats
have a better low light vision, because the same ray of light hits more photoreceptors,
but they have a less sharp image, because of this scatter of light.

The whole retinal network sits in front of the photoreceptors. The nerve fibers of the
ganglion cells have to go out of the eye and have to send signals to the brain. This
happens at a place where the light passes through the wall of the eye and the layer of
photoreceptors, in a region where light is not hitting any photoreceptors. This is called
the blind spot, and the location is called the optic disk. Thus, the retinal ganglion cell
(RGC) fibers lying on top cause the blind spot.


Glaucoma

There is a disease related to this, called glaucoma. This is caused by an increase of
pressure inside the eyes. There is fluid in front of the eye, and the eye has to be kept at
a certain pressure, because otherwise it will not be a balloon. This pressure should not
be too high. Sometimes, the mechanisms that regulate this pressure, the trabecular
meshwork, are somehow no longer capable of regulating the flow of the fluid. In the end,
there is an increase in pressure in the eye, so much that the optic nerve gets
compressed. This will cause damage, and you can lose part of your visual field. The
anatomy of the optic disk makes it that most of the time, you first lose your peripheral
vision. In a normal eye, you have just the blind spot. In glaucoma, you lose other parts
of your visual field.

The disease is progressive, but when it is in its early stages, you might not notice it.
Glaucoma patients often only notice it when it is too late, and when the progression
cannot be stopped (easily) anymore. The treatment is to release the pressure in the eye,
with eyedrops or surgery. Once the RGC fibers are lost, you cannot regain them. Patients
often don’t notice this until it is too late, so over the age of 40, it’s good to have your
eye pressure checked.

There are different types of glaucoma. There is an acute version, where the meshwork is
blocked for some acute reason, and you get a huge increase in optic pressure. The eye
gets really red and swollen, so you cannot see anything. More normal forms of glaucoma
are less noticeable.


Data compression

The bipolar cells and ganglion cells do some sort of preprocessing, before the signal from
rods and cones is passed to the brain. You can 130.000.000 photoreceptors in each eye
(130 megapixels), but you cannot send 130.000.000 RGC fibers through the optic nerve.
The optic nerve only contains one million fibers. There is a need for data compression.
The photoreceptors respond to light by hyperpolarization (the closing of the Na+
channels), and to dark by depolarization (opening of the Na+ channels). This is called a
graded potential signal. If you close the sodium channels, you get hyperpolarization of


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